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Pathogenesis of Stroke: Ischemia & Hemorrhage

Pathophysiology of Stroke Sid M. Shah, MD Assistant Residency Director Assistant Clinical Professor Department of Emergency Medicine Michigan State University East Lansing, MI. Pathogenesis of Stroke: Ischemia & Hemorrhage.

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Pathogenesis of Stroke: Ischemia & Hemorrhage

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  1. Pathophysiology of StrokeSid M. Shah, MDAssistant Residency DirectorAssistant Clinical ProfessorDepartment of Emergency MedicineMichigan State UniversityEast Lansing, MI

  2. Pathogenesis of Stroke:Ischemia & Hemorrhage • Ischemia: lack of circulating blood deprives the neurons of oxygen and nourishment • Hemorrhage: Extravascular release of blood causes damage by cutting off connecting pathways, resulting in local or generalized pressure injury

  3. Acute Ischemic Injury • The occlusion of a large vessel (such as MCA) is rarely complete and cerebral blood flow (CBF) depends on the degree of obstruction, and collateral circulation • Many factors influence progression and extent of ischemic injury

  4. Conditions influencing progression and extent of ischemic injury • Rate & duration of the ischemic event • Collateral circulation in the involved area of the brain • Systemic circulation & arterial blood pressure • Coagulation abnormalities • Temperature • Glucose

  5. Pathophysiology at Macro Tissue Level • Cerebral Blood Flow (CBF) • Ischemic Thresholds • Ischemic Penumbra and Window of Opportunity

  6. CBF & Ischemic Thresholds • Normal CBF 50-60 cc/100 g/minute • Varies in different regions of the brain • CBF 20-30cc/100g/min Loss of electrical activity • CBF 10 cc/100g/minNeuronal death

  7. Ischemic Penumbra & Window Of Opportunity • Ischemic zone that surrounds a central core of infarction with CBF of 25% to 50% of normal and loss of auto regulation • Viability of brain tissue is preserved if perfusion is restored within a critical time period (2 to 4 hours?)

  8. Microcellular Mechanisms of Neuronal Injury • Development of microcirculatory disturbances • Formation of micro thrombi • Accumulation of noxious metabolites • Interaction of endothelial cells with PMN leukocytes & platelets • PMNs trigger neuronal necrosis

  9. Microcellular Mechanisms of Neuronal Injury: Excitotoxicity • Ischemia depletes neuronal energy stores causing energy dependent membrane ion pumps to fail • This results in increased extracellular glutamate concentration • Release of excitotoxic Glutamate & Aspartate open up calcium channels resulting in influx of calcium, sodium and chloride and out flux of potassium causing irreversible neuronal damage

  10. Timing of Neuronal Death • Coagulation necrosis • Apoptosis

  11. Coagulation Necrosis • A process of cell death that evolves over 6 hours to 12 hours • Necrotic death is attributed to effects of physical, chemical and osmotic damage to the plasma membrane • Morphology of dying cells is distinct from that of cells dying from apoptosis

  12. Apoptosis • “Programmed cell death” triggered by ischemia, evolves over 2 hours • Ischemia activates latent “suicide” proteins that triggers an autolytic process mediated by DNA cleavage

  13. Major Categories of Ischemic Stroke • Thrombosis • Embolism • Global-Ischemic or Hypotensive Stroke

  14. Thrombotic Stroke • Atherosclerosis: the commonest pathology of vascular obstruction leading to thrombosis • Other pathological causes: • Fibro muscular dysplasia • Arteritis (Giant Cell & Takayasu) • Dissection of vessel wall and hemorrhage into atheromatous plaque • Hypercoaguability

  15. Embolic Stroke • Two most common sources of emboli: • Left sided cardiac chambers • Artery to artery stroke: as in detachment of a thrombus from ICA at the site of a plaque • Many embolic strokes become “hemorrhagic” • Generally “smaller” strokes than thrombotic strokes

  16. Embolism

  17. Ischemic Stroke Due To Hemodynamic Crisis: “Hypotensive Stroke” • Any event causing abrupt drop in blood pressure results in critical compromise of CBF (cerebral blood flow) and hence cerebral perfusion. • Sites affected by critically low CBF are located at the end of an arterial territory. Hence the term “watershed or boundary zone infarct.”

  18. Watershed Infarcts Resulting From Hemodynamic Crisis (Hypotensive Stroke)

  19. Selective Vulnerability of Neurons to Global Ischemia • Hippocampus: pyramidal cell layer • Cerebral cortex: Purkinje cell layer • Cerebellar cortex The increased vulnerability of these neurons is due to the abundance of neurotransmitter glutamate in these neurons

  20. Complications Of Restoration of Blood Flow: Hemorrhage and Edema • Arterial occlusion causes ischemia to capillaries, arterioles and vascular walls in addition to the deleterious effects on neurons • Hemorrhage (red infarcts) result when the fragile “ischemic” or “injured” vessels rupture after sudden restoration of blood flow • Vasogenic edema can also occur following a massive stroke or sudden restoration of blood flow to an ischemic area

  21. Factors Associated With Red Infarcts (Hemorrhagic Transformation) • Size of the infarct - bigger infarcts have a higher chance of becoming hemorrhagic • Richness of collateral circulation • Use of anti-coagulants • Treatment with thrombolytic agents

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